Abstract

The field stimulation-induced release of endogenous norepinephrine (studied by fluorescence histochemistry) and of exogenous H³-norepinephrine was investigated in the isolated rat iris. Isolated irides were incubated with H³-norepinephrine and then superfused with physiologic buffer before they were stimulated for 60 minutes. The stimulation caused a high release of H³-norepinephrine for 15 to 20 minutes which then declined. A slight reduction of the fluorescence intensity in the adrenergic nerves was observed. No release of norepinephrine occurred when C_a⁺⁺ was excluded from the buffer. Incubation with reserpine phosphate before the superfusion caused a high spontaneous tritium efflux, and this efflux was further enhanced by stimulation. These data confirm earlier in vivo findings that the depletion by reserpine can be influenced by nerve impulses. After reserpine and nialamide pretreatment the norepinephrine taken up into the nerves could not be released by stimulation in spite of a high intraneuronal concentration. One hour after treatment with H44/68 (a potent inhibitor of tyrosine hydroxylase) a higher stimulus-induced depletion of endogenous norepinephrine and a lower release of H³-norepinephrine was found, as compared to the release from irides of untreated rate. It may be that exogenous H³-norepinephrine is not available for stimulus-induced release to the same extent after H44/68 or that the nerves attempt to save as much transmitter as possible.